No evidence for a tumor necrosis factor alpha stimulated 2-methylaminoisobutyric acid uptake in hepatocyte monolayer

J Cell Physiol. 1995 Mar;162(3):422-6. doi: 10.1002/jcp.1041620314.

Abstract

This study investigates the short-term effects of glucagon and human recombinant tumor necrosis factor alpha (TNF alpha) singly and in association on 2-methylaminoisobutyric acid (MeAIB) transport in hepatocyte monolayers. As expected, glucagon induced a time-dependent stimulation of MeAIB transport. In our experimental conditions, TNF alpha did not induce cytolysis. A 2 hour exposure to TNF alpha (0.05-500 ng/l) with or without glucagon (10(-9) to 10(-6) M) did not modify the basal or glucagon-stimulated MeAIB transport. Varying the duration of exposure to TNF alpha 5 ng/l up to 6 h was equally ineffective. The presence of hydrocortisone potentiated the glucagon-stimulated transport, but TNF alpha remained ineffective. Finally, the association of interferon (IFN gamma) with TNF alpha and/or glucagon was unable to modify the transport activity. These data demonstrate that TNF alpha does not exert a direct effect on MeAIB transport in hepatocytes, at least on a short-term basis.

MeSH terms

  • Animals
  • Biological Transport / drug effects
  • Cells, Cultured
  • Glucagon / pharmacology
  • In Vitro Techniques
  • Interferon-gamma / pharmacology
  • Liver / metabolism*
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Serum Albumin / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*
  • beta-Alanine / analogs & derivatives*
  • beta-Alanine / metabolism

Substances

  • Serum Albumin
  • Tumor Necrosis Factor-alpha
  • beta-Alanine
  • 2,2-dimethyl-beta-alanine
  • Interferon-gamma
  • Glucagon